We proposed to continue our investigations into the hemodynamics of (a) Life-threatening sepsis, (b) Acute pancreatitis, (c) Gastrointestinal bleeding disorders. A. The altered hemodynamics of severe sepsis will be studied in an animal model already developed. Particular attention will be given to the "hyperdynamic state" with investigation of the distribution of this increased blood flow. Effort will be made to determine whether the increased flow is obligatory and hence whether it should be assisted or whether it could be usefully suppressed. B. Pancreatitis remains a largely unsolved clinical problem, taking a high toll in both morbidity and mortality. Little improvement has been made in its management in 10 to 20 years, and there is neither a clear understanding of its etiology nor a specific mode of therapy. We propose to examine the hypothesis that the name of he disease mau be misleading suggesting it to be of inflammatory origin. We will examine the hypothesis that it is not primarily an inflammatory disease, but is rather a disease resulting from a disordered hemodynamic environment. C. The effects of vasopressin given by various routes on splanchnic hemodynamics will be studied in normal and cirrhotic animals. The pathophysiology of therapeutic embolization will be examined. The relationship between gastric secretion, blood flow and H2 blockers will be determined. While this experimental attack may seem somewhat diffuse in attacking several different problems simultaneously, this has been the principal investigator's life-long area of research and the resources available to him as department head make the goals realistic.